We plan to investigate the metabolic basis of the neurological symptoms and psychosis which accompany the hereditary disease of acute porphyria. In this disease the patients in the acute phase excrete relatively large amounts of delta-aminolevulinic acid, the precursor of heme, chlorophyll, vitamin B12, etc. Since we have found that delta- aminolevulinic acid, a normal intermediate, kills at low concentration, the photosynthetic organism, Rhodopseudomonas spheroides, we further plan to investigate the mechanism of this killing action. It is our thesis that the biochemical lesion found with delta-aminolevulinic acid in the bacterial organism may be similar, it not the same, as that caused by the compound in a nerve cell. Another approach which may lead us to greater understanding of this disease is a study in depth of the enzymes concerned with the synthesis of delta-aminolevulinic acid and its conversion to the pyrrole, porphobilinogen. We plan to continue our efforts in determining the primary, quaternary, and tertiary structures of delta-aminolevulinic acid dehydratase especially since we have crystallized it and have determined its subunit structure.